Vitamins, Folic Acid and the Cause and Prevention of Neural Tube Defects

  1. Gregory Bock and
  2. Joan Marsh
  1. Mary J. Seller

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514559.ch10

Ciba Foundation Symposium 181 - Neural Tube Defects

Ciba Foundation Symposium 181 - Neural Tube Defects

How to Cite

Seller, M. J. (2007) Vitamins, Folic Acid and the Cause and Prevention of Neural Tube Defects, in Ciba Foundation Symposium 181 - Neural Tube Defects (eds G. Bock and J. Marsh), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514559.ch10

Author Information

  1. Division of Medical & Molecular Genetics, United Medical & Dental Schools of Guy's & St Thomas's Hospitals, 7/8th Floors, Guy's Tower, Guy's Hospital, London Bridge, London SE1 9RT, UK

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471941729

Online ISBN: 9780470514559

SEARCH

Keywords:

  • vitamins;
  • folic acid;
  • neural tube defects;
  • protein synthesis;
  • red blood cells

Summary

Primary prevention of neural tube defects has been demonstrated in humans by maternal therapy with multivitamins and folic acid or folic acid alone. It has also been shown in several animal models of neural tube defects. One of these, the curly tail mouse, has been used extensively to study which agents will prevent neural tube defects in embryos when administered to the mother in early pregnancy. Prevention is achieved with retinoic acid, inositol and the DNA inhibitors hydroxyurea, mitomycin C, 5-fluorouracil and cytosine arabinoside. In no case were neural tube defects prevented in every embryo. A possible preventive effect was seen with riboflavin, vitamin C and vitamin D2. Despite the use of a variety of dose levels, no prevention was achieved with folk acid, folinic acid, Pregnavite Forte F® tablets, pyridoxine or vitamin B12, or triamcinolone and cycloheximide (inhibitors of mRNA and protein synthesis, respectively), zinc, homocysteine, methionine and thymidine. Various studies have investigated whether there is a biochemical lesion in folate metabolism in women who have had children with neural tube defects. While there is no difference in their dietary intake of folate compared with control patients, the correlation between their dietary folate and the level of folate in both serum and red blood cells is distorted. Also they are less efficient at raising their folate levels after a folate load. The effects are minor but may hint at a lesion which, if identified, could act as a marker for ‘at risk’ women.